MIR489

MIR489
Identifiers
Aliases	MIR489 , MIRN489, hsa-mir-489, mir-489, microRNA 489
External IDs	OMIM: 614523 GeneCards: MIR489
Gene location (Human) Chr. Chromosome 7 (human) [1] Band 7q21.3 Start 93,483,936 bp [1] End 93,484,019 bp [1]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in kidney amygdala nucleus accumbens ascending aorta minor salivary gland skin of abdomen dorsolateral prefrontal cortex spleen colon n/a More reference expression data BioGPS n/a
Orthologs Species Human Mouse Entrez 574442 n/a Ensembl ENSG00000207656 n/a UniProt n a n/a RefSeq (mRNA) n/a n/a RefSeq (protein) n/a n/a Location (UCSC) Chr 7: 93.48 – 93.48 Mb n/a PubMed search [2] n/a
Wikidata
View/Edit Human

MicroRNA 489 is a miRNA that in humans is encoded by the MIR489 gene. ^[3]

Function

microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into an RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop. miR-489 acts as tumor suppressor miRNA in breast cancer by inhibiting various oncogenic signaling pathway. It has been demonstrated miR-489 target HER2 and LAPTM4b by directly binding to their 3'UTR. Role of miR-489 has been studied in autochatothus MMTV-Her2 mouse model. ^[4]

References

1. GRCh38: Ensembl release 89: ENSG00000207656 - Ensembl, May 2017
2. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
3. "Entrez Gene: MicroRNA 489".
4. Patel Y, Shah N, Lee JS, Markoutsa E, Jie C, Liu S, Botbyl R, Reisman D, Xu P, Chen H (April 2016). "A novel double-negative feedback loop between miR-489 and the HER2-SHP2-MAPK signaling axis regulates breast cancer cell proliferation and tumor growth". Oncotarget. 7 (14): 18295–308. doi:10.18632/oncotarget.7577. PMC   4951289 . PMID   26918448.

Further reading

• Kikkawa N, Hanazawa T, Fujimura L, Nohata N, Suzuki H, Chazono H, Sakurai D, Horiguchi S, Okamoto Y, Seki N (2010). "miR-489 is a tumour-suppressive miRNA target PTPN11 in hypopharyngeal squamous cell carcinoma (HSCC)". Br. J. Cancer. 103 (6): 877–84. doi:10.1038/sj.bjc.6605811. PMC   2966617 . PMID   20700123.
• Wu H, Xiao Z, Zhang H, Wang K, Liu W, Hao Q (2014). "MiR-489 modulates cisplatin resistance in human ovarian cancer cells by targeting Akt3". Anticancer Drugs. 25 (7): 799–809. doi:10.1097/CAD.0000000000000107. PMID   24686007. S2CID   205525849.
• Jiang L, He D, Yang D, Chen Z, Pan Q, Mao A, Cai Y, Li X, Xing H, Shi M, Chen Y, Bruce IC, Wang T, Jin L, Qi X, Hua D, Jin J, Ma X (2014). "MiR-489 regulates chemoresistance in breast cancer via epithelial mesenchymal transition pathway". FEBS Lett. 588 (11): 2009–15. doi: 10.1016/j.febslet.2014.04.024 . PMID   24786471. S2CID   21988931.
• Patel Y, Soni M, Awagulerwitsch A, Kern MJ, Liu S, Shah N, Singh UP, Chen H (August 2018). "Overexpression of miR-489 derails mammary hierarchy structure and inhibits HER2/neu-induced tumorigenesis". Oncogene. 38 (3): 445–453. doi:10.1038/s41388-018-0439-1. PMC   6338493 . PMID   30104710.
• Patel Y, Lee JS, Chen H (June 2016). "Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization". Journal of Visualized Experiments (112). doi:10.3791/53928. PMC   4922489 . PMID   27341462.

This article incorporates text from the United States National Library of Medicine, which is in the public domain.